ArticleGenetics2017
Rewiring of Signaling Networks Modulating Thermotolerance in the Human Pathogen Cryptococcus neoformans.
Article in Genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- Article
- Article
- Heat Shock Proteins in Medically Relevant Fungal Pathogens: From Molecular Chaperones to Virulence Factors and Therapeutic Targets.Journal of fungi (Basel, Switzerland) · 2026Review
- Systematic Profiling of Essential Fungal Transcription Factors Uncovers Ezt1 as a Central Pathobiological and Morphogenic Regulator inResearch square · 2026Article
- Ricin B lectin-like proteins mediate thermotolerance, cell wall integrity, and fungal virulence inCell surface (Amsterdam, Netherlands) · 2026Article
- Systematic Profiling of Essential Fungal Transcription Factors Uncovers Ezt1 as a Central Pathobiological and Morphogenic Regulator inbioRxiv : the preprint server for biology · 2026Article
- Conserved and rewired MAPK networks in human fungal pathogens.FEMS yeast research · 2026Review
- Deciphering the role of the Sch9 serine/threonine kinase inFrontiers in fungal biology · 2026Article
- Temperature and genetic background drive mobilization of diverse transposable elements in a global human fungal pathogen.PLoS genetics · 2026Article
- Pathogenic Fungal Sensing and Responses to Stressful Host Environments.Annual review of microbiology · 2025Review
- Natural compounds from freshwater mussels disrupt fungal virulence determinants and influence fluconazole susceptibility in the presence of macrophages inMicrobiology spectrum · 2024Article
- Cryptococcus neoformans adapts to the host environment through TOR-mediated remodeling of phospholipid asymmetry.Nature communications · 2023Article
- Cryptococcus neoformans requires the TVF1 gene for thermotolerance and virulence.Medical mycology · 2023Article
- Adenylyl-Sulfate Kinase (Met14)-Dependent Cysteine and Methionine Biosynthesis Pathways Contribute Distinctively to Pathobiological Processes in Cryptococcus neoformans.Microbiology spectrum · 2023Article
- Differentiated extracts from freshwater and terrestrial mollusks inhibit virulence factor production in Cryptococcus neoformans.Scientific reports · 2023Article
- Mitochondria in Cryptococcus: an update of mitochondrial transcriptional regulation in Cryptococcus.Current genetics · 2023Review
- Genome-wide analysis of heat stress-stimulated transposon mobility in the human fungal pathogenProceedings of the National Academy of Sciences of the United States of America · 2023Article
- The function and regulation of heat shock transcription factor inFrontiers in cellular and infection microbiology · 2023Review
- Regulatory basis for reproductive flexibility in a meningitis-causing fungal pathogen.Nature communications · 2022Article
- Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Thermotolerance is a crucial virulence attribute for human pathogens, including the fungus Cryptococcus neoformans that causes fatal meningitis in humans. Loss of the protein kinase Sch9 increases C. neoformans thermotolerance, but its regulatory mechanism has remained unknown. Here, we studied the Sch9-dependent and Sch9-independent signaling networks modulating C. neoformans thermotolerance by using genome-wide transcriptome analysis and reverse genetic approaches. During temperature upshift, genes encoding for molecular chaperones and heat shock proteins were upregulated, whereas those for translation, transcription, and sterol biosynthesis were highly suppressed. In this process, Sch9 regulated basal expression levels or induced/repressed expression levels of some temperature-responsive genes, including heat shock transcription factor (HSF1) and heat shock proteins (HSP104 and SSA1). Notably, we found that the HSF1 transcript abundance decreased but the Hsf1 protein became transiently phosphorylated during temperature upshift. Nevertheless, Hsf1 is essential for growth and its overexpression promoted C. neoformans thermotolerance. Transcriptome analysis using an HSF1 overexpressing strain revealed a dual role of Hsf1 in the oxidative stress response and thermotolerance. Chromatin immunoprecipitation demonstrated that Hsf1 binds to the step-type like heat shock element (HSE) of its target genes more efficiently than to the perfect- or gap-type HSE. This study provides insight into the thermotolerance of C. neoformans by elucidating the regulatory mechanisms of Sch9 and Hsf1 through the genome-scale identification of temperature-dependent genes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.